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Conn’s Syndrome: An Unusual Cause of Periodic Paralysis

Primary hyperaldosteronism, also known as Conn’s syndrome, is characterized by an independent and excessive aldosterone production in the adrenal cortex, causing hypernatremia, arterial hypertension, and, in some cases, potentially severe hypokalemia can occur. We report a case of a 45-year-old Cauc...

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Detalles Bibliográficos
Autores principales: Balhana, Sílvia, Pina, Henrique, Machete, Madalena, Aragüés, José Maria, Noronha, Carla
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9180667/
https://www.ncbi.nlm.nih.gov/pubmed/35702451
http://dx.doi.org/10.7759/cureus.24880
Descripción
Sumario:Primary hyperaldosteronism, also known as Conn’s syndrome, is characterized by an independent and excessive aldosterone production in the adrenal cortex, causing hypernatremia, arterial hypertension, and, in some cases, potentially severe hypokalemia can occur. We report a case of a 45-year-old Caucasian woman, with a history of obesity and hypertension, who presented to the emergency room with a four-week evolution history of myalgia and ascending muscle weakness eventually resulting in tetraparesis. The initial blood analysis showed severe hypokalemia (1.5 mmol/L). Further laboratory studies revealed an elevated plasma aldosterone level with low renin activity, and thyroid function tests were consistent with mild primary hyperthyroidism. CT scan showed a nodular lesion in the left adrenal gland. A saline suppression test confirmed that aldosterone secretion and renin activity were not suppressed. Regression of tetraparesis was noted with vigorous potassium supplementation. A laparoscopic left adrenalectomy was performed, with consequent normalization of hypokalemia, without the need for supplementation. Periodic paralysis (PP) are a rare group of neuromuscular diseases that occur due to the affection of the ion channels of the skeletal muscle. Most cases are hereditary; nonetheless, secondary causes of PP have been reported in the literature.  This case illustrates an unusual and severe presentation of primary hyperaldosteronism manifested by PP. The concomitant changes in thyroid function raised the possibility that we are facing the clinical influence of another rare entity: thyrotoxic hypokalemic PP. However, the resolution of hypokalemia after the removal of adrenal adenoma supported the major contribution of hyperaldosteronism.